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BALB/c

About: BALB/c is a research topic. Over the lifetime, 4842 publications have been published within this topic receiving 112066 citations. The topic is also known as: Mice, Inbred BALB C.


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Journal ArticleDOI
TL;DR: Lymphoid cells from many normal mice of a variety of inbred strains were found to have reactivity, in a 51Cr release cytotoxicity assay, against several syngeneic and allogeneic tumors, apparently associated with expression of murine endogenous type‐C viruses.
Abstract: Lymphoid cells from many normal mice of a variety of inbred strains were found to have reactivity, in a 51Cr release cytotoxicity assay, against several syngeneic and allogeneic tumors. Very high reactivity was seen with effector cells from athymic nude mice, which was consistent with other evidence that the reactivity was not T-cell dependent. Target cells susceptible to lysis included tumors induced by oncogenic type-C viruses but also tumors induced by other means and expressing endogenous type-C viruses. The levels of natural reactivity were influenced by age, with highest cytotoxicity produced by cells from 5- to 8-week-old mice. Lymph-node cells, spleen cells, peritoneal exudate cells and peripheral blood lymphocytes all had cytotoxic reactivity. The specificity of the reactions was analyzed in detail by ana inhibition assay. Evidence was obtained for natural reactivty against several different antigens, each apparently associated with expression of murine endogenous type-C viruses.

1,314 citations

Journal ArticleDOI
TL;DR: Conjugation of TNP directly to the erythrocyte surface by use of TNBS resulted in a stable reagent that permitted a study of the antihapten response to TNP-KLH and indicated the higher binding affinity of secondary antibody.
Abstract: SummaryA technique was developed for the detection of individual cells producing anti-TNP antibody by the hemolytic plaque technique. Conjugation of TNP directly to the erythrocyte surface by use of TNBS resulted in a stable reagent that permitted a study of the antihapten response to TNP-KLH. It was possible to induce a primary anti-TNP response with soluble TNP-KLH but the response was greater when the immunogen was made particulate by coating it onto bentonite. Both primary and secondary responding cells (those brought out by antiglobulin serum) were inhibited by TNP-BSA added to the plating medium but at an equivalent concentration of hapten only the secondary cells were completely inhibited. This was interpreted to indicate the higher binding affinity of secondary antibody.Author's note. As we were in process of submitting this manuscript, we became aware of an abstract which indicated that responses of similar magnitude to those reported here with TNP could be obtained in Balb/c mice to DNP using a ...

724 citations

Journal Article
TL;DR: Karyotype studies show that L10A, K46, X16C, and BALENLM 17 are hyperdiploid to hypotetraploid, and A20 and M12 have near diploid chromosome numbers.
Abstract: Five spontaneously derived BALB/c tumors and one 1-ethyl-1-nitrosourea induced BALB/c tumor (BALENLM 17), have been established in culture and characterized according to their surface markers. K46, X16C, L10A, and BALENLM 17 are IgM+, IgG-, IgA-, Ig+ (staining with polyvalent anti-Ig), Ia+, Fc receptor+ and complement receptor-. A20 is IgM-, IgG-, IgA-, Ig+, Ia+, Fc receptor+, and complement receptor-. M12 is IgM-, IgG-, IgA-, Ig±, Ia-, Fc receptor+ and complement receptor-. All these lines are Thy 1.2 antigen negative, do not phagocytize latex particles, and grow as stationary suspension cultures. Therefore these six BALB/c lymphoid lines are presumably of B cell origin at various stages of differentiation. All these lines except X16C are tumorigenic in mice within a short period of time and have relatively short generation times in the range of 18 to 26 hr. Karyotype studies show that L10A, K46, X16C, and BALENLM 17 are hyperdiploid to hypotetraploid. A20 and M12 have near diploid chromosome numbers.

630 citations

Journal ArticleDOI
25 Sep 2020-Science
TL;DR: A mouse model in which a SARS-CoV-2 strain was infectious and could cause an inflammatory response and moderate pneumonia is developed, and a panel of adaptive mutations potentially associated with the increased virulence are revealed.
Abstract: The ongoing coronavirus disease 2019 (COVID-19) pandemic has prioritized the development of small-animal models for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We adapted a clinical isolate of SARS-CoV-2 by serial passaging in the respiratory tract of aged BALB/c mice. The resulting mouse-adapted strain at passage 6 (called MASCp6) showed increased infectivity in mouse lung and led to interstitial pneumonia and inflammatory responses in both young and aged mice after intranasal inoculation. Deep sequencing revealed a panel of adaptive mutations potentially associated with the increased virulence. In particular, the N501Y mutation is located at the receptor binding domain (RBD) of the spike protein. The protective efficacy of a recombinant RBD vaccine candidate was validated by using this model. Thus, this mouse-adapted strain and associated challenge model should be of value in evaluating vaccines and antivirals against SARS-CoV-2.

623 citations

Journal ArticleDOI
TL;DR: It is believed that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease and stress the effect of genetic background on the outcome of DSS provocation.
Abstract: Exposure to dextran sulfate sodium (DSS) induces acute colitis, which is normally resolved after DSS removal. To study chronicity, mice are typically subjected to three to five cycles of weekly DSS exposures, each followed by a 1- to 2-wk rest period. Here, we describe a novel and convenient way of inducing chronic, progressive colitis by a single exposure to DSS. C57BL/6 mice exposed to DSS for 5 days developed acute colitis that progressed to severe chronic inflammation. The plasma haptoglobin levels remained high during the chronic phase, showing that the inflammation was active. Surprisingly, the mice regained their original weight along with the progression of colitis, and the only apparent symptom was loose feces. Histopathological changes 4 wk after DSS removal were dense infiltrates of mononuclear cells, irregular epithelial structure, and persistent deposits of collagen. A progressive production of the cytokines IL-1β, IL-12 p70, and IL-17 correlated with the extensive cellular infiltration, whereas high IFN-γ production was mainly found late in the chronic phase. Similar to C57BL/6 mice, BALB/c mice exposed to 5 days of DSS developed acute colitis as previously described. The acute colitis was accompanied by elevated plasma levels of haptoglobin and increased colonic levels of IL-1α/β, IL-6, IL-18, and granulocyte colony-stimulating factor. However, soon after DSS removal, BALB/c mice recovered and were symptom free within 2 wk and completely recovered 4 wk after DSS removal in terms of histopathology, haptoglobin levels, and local cytokine production. In summary, these data stress the effect of genetic background on the outcome of DSS provocation. We believe that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease.

538 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202329
202258
2021119
2020143
2019148
2018133